We reported that human platelets aggregate when decompressed by reduced barometric pressure to 253 torr and that this aggregation was inhibited by menthol and methone at 10 mM and by thymol, an aromatic derivative of menthol, at 5 MuM. A theory of spontaneous aggregation of human platelets by decompression was derived from our observation that the molecular volume of activation of fibrin polymerization is a large positive number. Therefrom, it was deduced that the rate of fibrin polymerization could be accelerated by decompression. This was experimentally tested and confirmed by producing spontaneous aggregation of platelets decompressed by various means. The corollary to the theory is that platelets generally do not aggregate when compressed. Recently, we confirmed our previous observation that the rate of fibrin polymerization was essentially doubled at 1/2 atm compared to the control at 1 atm. Furthermore, it was found that fibrin polymer "melts" under high hydraulic pressure (10,000 psi). Fibrin polymerization appears, therefore, to be a reversible process as predicted by theory (Murayama and Nakada). The pressure effects on fibrin and platelet aggregation demonstrate that the underlying mechanisms involve electric constriction and that electrically charged residues are involved. The design of future experiments is directed towards solving the electrostriction problem(s) in fibrin polymerization as related to platelet aggregation.